Estimates of mean alveolar PCO2 during steady-state exercise in man: A theoretical study
✍ Scribed by K.B. Saunders; A.R.C. Cummin
- Book ID
- 104154996
- Publisher
- Elsevier Science
- Year
- 1992
- Tongue
- English
- Weight
- 958 KB
- Volume
- 159
- Category
- Article
- ISSN
- 0022-5193
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✦ Synopsis
The partial pressure of carbon dioxide in arterial blood is an important operator in the control of breathing, by actions on peripheral and central chemoreceptors. In experiments on man we must often assume that lung alveolar PCO2 equals arterial PCO2 and obtain estimates of the former derived from measurements in expired gas sampled at the mouth. This paper explores the potential errors of such estimates, which are magnified during exercise. We used a published model of the cardiopulmonary system to simulate various levels of exercise up to 300 W. We tested three methods of estimating mean alveolar PCO2 (PACO~) against the true value derived from a time average of the within-breath oscillation in steady-state exercise. We used both sinusoidal and square-wave ventilatory flow wave forms.
Over the range 33-133 W end-tidal PCO2 (PetCO2) overestimated P,~CO2 progressively with increasing workload, by about 4 mmHg at 133 W with normal respiratory rate for that load. PCO2 by a graphical approximation technique (PgCO2 ; "graphical method") underestimated PACO2 by 1-2 mmHg. PCO2 from an experimentally obtained empirical equation (PnjCO2 ; "empirical method") overestimated PACO2 by 0-5-I.0 mmHg. Graphical and empirical methods were insensitive to alterations in cardiac output or respiratory rate. End-tidal PCO2 was markedly affected by respiratory rate during exercise, the overestimate of P,~CO2 increasing if respiratory rate was slowed. An increase in anatomical dead space with exercise tends to decrease the error in PetCO2 and increase the error in the graphical method. Changes in the proportion of each breath taken up by inspiration make no important difference, and changes in functional residual capacity, while important in principle, are too small to have any major effect on the estimates. Changes in overall alveolar ventilation which alter steady-state P,~CO2 over a range of 30-50 mmHg have no important effect. At heavy work loads (200-300W), PctCO2 grossly overestimates by 6-9 mmHg. The graphical method progressively underestimates, by about 5 mmHg at 300 W.
A simulated CO2 response (the relation between ventilation and increasing PCO2) performed at 100 W suggests that a response slope close to the true one can be obtained by using any of the three methods. The graphical method gave results closest to the true absolute values. Either graphical or empirical methods should be satisfactory for detecting experimentally produced changes in PACO2 during steadystate exercise, to make comparisons between different steady-state exercise loads, and to assess CO2 response in exercise. The rate and load dependency of PctCO2 makes it unsuitable for these purposes.